The Experts below are selected from a list of 1473 Experts worldwide ranked by ideXlab platform

Cheramadathikudyil S. Paulose - One of the best experts on this subject based on the ideXlab platform.

  • Brain Stem GABA Receptor Functional Regulation During Rat Liver Cell Proliferation
    Neurochemical Research, 2002
    Co-Authors: Mangatt P. Biju, Sulaiman Pyroja, Neelimmathara V. Rajeshkumar, Cheramadathikudyil S. Paulose
    Abstract:

    GABAergic alterations in brain stem during Compensatory Hyperplasia after partial hepatectomy (PH), lead nitrate (LN)-induced direct Hyperplasia, and N -nitrosodiethylamine (NDEA)-induced neoplasia in liver were investigated. GABA content decreased in brain stem of PH- and NDEA-treated rats while it increased in LN-treated rats. GABA_A receptor number and affinity in brain stem membrane preparations of rats showed a significant decrease in PH- and NDEA-treated rats. The GABA_B receptor number increased in PH- and NDEA-treated rats with an increase in affinity. The results of the present study indicate that liver cell proliferation is influencing the brain stem GABAergic neurotransmission and these changes regulate the hepatic proliferation through the sympathetic stimulation.

  • Hypothalamic GABA receptor functional regulation and liver cell proliferation
    Molecular and Cellular Biochemistry, 2001
    Co-Authors: Mangatt P. Biju, Sulaiman Pyroja, Neelimmathara V. Rajeshkumar, Cheramadathikudyil S. Paulose
    Abstract:

    GABAergic alterations in hypothalamus during Compensatory Hyperplasia after partial hepatectomy (PH), lead nitrate (LN) induced direct Hyperplasia and N -nitrosodiethylamine (NDEA) induced neoplasia in liver were investigated. Serum GABA levels were increased in all 3 experimental groups compared with the control. GABA content decreased in hypothalamus of PH and NDEA treated rats, while it increased in LN treated rats. GABA_A receptor number and affinity in hypothalamic membrane preparations of rats showed a significant decrease in PH and NDEA treated rats, while in LN treated rats the affinity increased without any change in the receptor number. The GABA_B receptor number increased in PH and NDEA treated rats, while it decreased in LN treated rats. The affinity of the receptor also increased in NDEA treated rats. Plasma NE levels showed significant increase in PH and NDEA rats compared with the control while it decreased in LN treated rats. The results of the present study suggests that liver cell proliferation is influencing the hypothalamic GABAergic neurotransmission and these changes regulate the hepatic proliferation through the sympathetic stimulation.

George K. Michalopoulos - One of the best experts on this subject based on the ideXlab platform.

  • Plasma levels of HGF in rats treated with tumor promoters.
    Carcinogenesis, 1992
    Co-Authors: Pamela Lindroos, W.h. Tsai, R. Zarnegar, George K. Michalopoulos
    Abstract:

    Hepatocyte growth factor (HGF), mol. wt 105,000 is a potent mitogen for hepatocytes. HGF is strongly associated with Compensatory regeneration in the liver after two-thirds partial hepatectomy and carbon tetrachloride administration. Plasma levels of HGF increase markedly during early stages of Compensatory Hyperplasia caused by these treatments. This is followed by an increase in HGF mRNA in the liver. This is in contrast to other growth factors for liver (epidermal growth factor, transforming growth factor alpha and acidic fibroblast growth factor) whose levels in plasma remain virtually undetectable during Compensatory Hyperplasia. We have shown that during augmentative Hyperplasia caused by the tumor promoters alpha-hexachlorocyclohexane, phenobarbital and ciprofibrate, plasma levels of HGF also increase. This increase of HGF occurs during the transient wave of DNA synthesis caused by administration of these xenobiotics, providing further support for HGF as being the stimulator of DNA synthesis during both augmentative and Compensatory Hyperplasia.

Mangatt P. Biju - One of the best experts on this subject based on the ideXlab platform.

  • Brain Stem GABA Receptor Functional Regulation During Rat Liver Cell Proliferation
    Neurochemical Research, 2002
    Co-Authors: Mangatt P. Biju, Sulaiman Pyroja, Neelimmathara V. Rajeshkumar, Cheramadathikudyil S. Paulose
    Abstract:

    GABAergic alterations in brain stem during Compensatory Hyperplasia after partial hepatectomy (PH), lead nitrate (LN)-induced direct Hyperplasia, and N -nitrosodiethylamine (NDEA)-induced neoplasia in liver were investigated. GABA content decreased in brain stem of PH- and NDEA-treated rats while it increased in LN-treated rats. GABA_A receptor number and affinity in brain stem membrane preparations of rats showed a significant decrease in PH- and NDEA-treated rats. The GABA_B receptor number increased in PH- and NDEA-treated rats with an increase in affinity. The results of the present study indicate that liver cell proliferation is influencing the brain stem GABAergic neurotransmission and these changes regulate the hepatic proliferation through the sympathetic stimulation.

  • Hypothalamic GABA receptor functional regulation and liver cell proliferation
    Molecular and Cellular Biochemistry, 2001
    Co-Authors: Mangatt P. Biju, Sulaiman Pyroja, Neelimmathara V. Rajeshkumar, Cheramadathikudyil S. Paulose
    Abstract:

    GABAergic alterations in hypothalamus during Compensatory Hyperplasia after partial hepatectomy (PH), lead nitrate (LN) induced direct Hyperplasia and N -nitrosodiethylamine (NDEA) induced neoplasia in liver were investigated. Serum GABA levels were increased in all 3 experimental groups compared with the control. GABA content decreased in hypothalamus of PH and NDEA treated rats, while it increased in LN treated rats. GABA_A receptor number and affinity in hypothalamic membrane preparations of rats showed a significant decrease in PH and NDEA treated rats, while in LN treated rats the affinity increased without any change in the receptor number. The GABA_B receptor number increased in PH and NDEA treated rats, while it decreased in LN treated rats. The affinity of the receptor also increased in NDEA treated rats. Plasma NE levels showed significant increase in PH and NDEA rats compared with the control while it decreased in LN treated rats. The results of the present study suggests that liver cell proliferation is influencing the hypothalamic GABAergic neurotransmission and these changes regulate the hepatic proliferation through the sympathetic stimulation.

M. R. Alison - One of the best experts on this subject based on the ideXlab platform.

  • The many ways to mend your liver: A critical appraisal.
    International journal of experimental pathology, 2018
    Co-Authors: M. R. Alison
    Abstract:

    In the latter half of the 20th century, our understanding of mammalian liver regeneration was shaped by the manner of Compensatory Hyperplasia occurring after a partial rat liver resection. This response involves almost all hepatocytes and thus is unlikely to be the outcome of the multiple cycling of a small stem cell population. It was most intense in the outer third of lobule, the location closest to the afferent arterial blood supply. With the advent of heritable genetic labelling techniques, usually applied to mice, hitherto unrecognized hepatocytes with clonogenic potential have been discovered, contributing to homoeostatic renewal and/or regenerative responses after tissue loss. This review combines observations from cell lineage tracing studies with other data to summarize the Four proposed anatomical locations for hepatocyte stem cells: the periportal zone, the pericentral zone, a randomized distribution and finally within the intrahepatic biliary tree. As in other endodermal-derived tissues, it appears that there are both homoeostatic stem cells and regenerative stem cells, while some normally homoeostatic stem cells can become more active to boost regeneration.

  • Liver cell Hyperplasia: on the suitability of using the metaphase-arrest technique.
    Cell and tissue kinetics, 2008
    Co-Authors: J. A. Alabi, M. R. Alison
    Abstract:

    This study has explored the possibility of applying the metaphase-arrest method with colchicine to two models of induced liver growth in the rat, regenerative growth and phenobarbital-induced growth. At a dosage of 0.5 mg/kg body weight (BW), colchicine caused a linear accumulation of mitoses for up to 90 min when administered at 3 days after the start of phenobarbital treatment; however these mitoses included a number of anaphases and telophases. No anaphase escape was seen when this dose of colchicine was given at various times after partial hepatectomy, though the arrested mitoses were invariably more fragmented and some may have even degenerated beyond recognition as early as 90 min after injection. It is concluded that the optimal dose of stathmokinetic agent is heavily dependent on the relative liver weight, and thus would change continuously during Compensatory Hyperplasia.

James M. Crawford - One of the best experts on this subject based on the ideXlab platform.

  • Vascular Disorders of the Liver
    Clinics in liver disease, 2010
    Co-Authors: James M. Crawford
    Abstract:

    Hepatic vascular disorders are a set of conditions that may be acute, or may be insidious and subclinical for many years. They can be organized into 3 categories: obstruction to hepatic vascular inflow, obstruction to blood flow through the liver, and obstruction to hepatic vascular outflow. In the first category are portal vein thrombosis, hepatic artery thrombosis, and presinusoidal causes of vascular obstruction. In the second category are sickle cell disease, disseminated intravascular coagulation, intrasinusoidal malignancy, and infection. In the third category are macroscopic hepatic venous thrombosis, thrombosis of the retrohepatic inferior vena cava, and venoocclusive disease. There are 2 nodular conditions of the liver that are not neoplastic but the result of occlusion of hepatic vasculature with Compensatory Hyperplasia of well-vascularized parenchyma. Hepatic vascular disorders constitute a heterogeneous group of conditions that must be considered in the differential diagnosis of any patient with hepatic compromise.